Clinical Assessment — Raj, 25Y/M | LCH History + Current Presentation

⚠️ Important disclaimer: This analysis is for educational and informational purposes only. It does not constitute a medical diagnosis or replace evaluation by a qualified physician. The findings described here are urgent — please take Raj to a specialist (haematologist/oncologist or endocrinologist) without delay.

Summary of Key Findings from the Report

Abnormal Results at a Glance

Clinical Synthesis and Diagnosis

The Central Picture: LCH Relapse with Central Diabetes Insipidus

1. Polydipsia + polyuria (drinks a lot of water, urinates frequently)
2. New soft tissue swelling on the forehead (calvarial/skull lesion)
3. Severe weakness and inability to eat

"In about 50% of cases, involvement of the posterior pituitary stalk of the hypothalamus leads to diabetes insipidus. The combination of calvarial bone defects, diabetes insipidus, and exophthalmos is referred to as the Hand-Schüller-Christian [syndrome]." — Robbins & Kumar Basic Pathology, p. 424

"Granulomatous diseases, such as Langerhans cell histiocytosis, sarcoidosis, tuberculosis, and leukemic infiltrates of the hypothalamus can cause diabetes insipidus by destroying vasopressin cells." — Goldman-Cecil Medicine, p. 2423

Secondary Diagnosis: Pituitary–Hypothalamic Axis Damage (Hypopituitarism)

Supporting Abnormalities

Most Likely Diagnosis

LCH relapse with hypothalamic-pituitary infiltration, presenting as:

• Central diabetes insipidus (polyuria, polydipsia, mild hypernatremia)
• Hypogonadotropic hypogonadism (testosterone severely low → fatigue, weakness, anorexia)
• Active calvarial lesion (forehead swelling = bone involvement, a classic LCH site)
• Iron-deficiency anemia (secondary to chronic disease + poor nutrition)
• Atherogenic dyslipidemia (driven by hypogonadism + metabolic state)
• Vitamin D deficiency

Urgent Investigations Required

Treatment Plan

1. Central Diabetes Insipidus — URGENT

• Intranasal: 10–40 mcg/day in 1–2 divided doses
• Or oral tablet: 0.1–0.4 mg twice/thrice daily
• Monitor urine output, serum sodium closely to avoid hyponatremia during titration

Goldman-Cecil: "Treatment... can consist of replacement of vasopressin via synthetic vasopressin analogues in central diabetes insipidus."

2. LCH Systemic Treatment (Relapsed/Refractory)

• Cladribine (2-CDA) ± cytarabine (Ara-C) — most used for multisystem/CNS LCH relapse
• Vinblastine + prednisolone — used in frontline, less favored in CNS relapse

• Vemurafenib or Dabrafenib ± Trametinib (BRAF/MEK inhibitors) — highly effective in BRAF-mutated LCH, including CNS disease; emerging as standard for CNS-LCH relapse

• MEK inhibitors (trametinib, cobimetinib) may still be active given MAP kinase pathway activation in virtually all LCH

3. Hypogonadism

• Testosterone replacement therapy (transdermal gel or IM injection) after confirming LH/FSH levels
• This will directly help with fatigue, weakness, appetite, and mood

4. Iron Deficiency Anemia

• Oral ferrous sulfate 200 mg TDS with vitamin C (ascorbic acid) between meals
• If GI intolerance or severe: IV ferric carboxymaltose

5. Vitamin D Deficiency

• Vitamin D3 (cholecalciferol) 60,000 IU weekly for 8–12 weeks, then maintenance 1,000–2,000 IU/day
• Recheck 25-OH Vit D at 3 months

6. Dyslipidemia

• Address root cause first (testosterone deficiency, active disease)
• If persists after treatment: consider statin therapy (e.g., rosuvastatin 10 mg) given LDL 168 mg/dL
• Dietary modification: reduce saturated fats, increase fibre

7. Nutrition Support

• High-protein, calorie-dense diet
• Nutritional supplements (ensure/protein shakes) given anorexia
• Consider dietician referral

8. Hyperuricemia

• Increase hydration (already occurring via DI, but monitor)
• Allopurinol if symptomatic gout develops or uric acid rises further after treatment

Why This Is Not Diabetes Mellitus

Summary Action Plan

URGENT (within 24–48 hours):
├── MRI pituitary with gadolinium
├── Urine and serum osmolality
├── Full pituitary axis hormones (LH, FSH, cortisol, ACTH, prolactin, IGF-1)
├── Start desmopressin if DI confirmed
└── Oncology/haematology referral for LCH relapse workup

SHORT-TERM (1–2 weeks):
├── Skull CT / bone survey
├── Biopsy of forehead swelling
├── BRAF V600E mutation testing
├── FDG-PET for disease extent
└── Start iron, Vitamin D supplementation

ONGOING:
├── Testosterone replacement (after axis evaluation)
├── LCH-directed systemic therapy (per oncologist)
├── Lipid management
└── Nutritional support

• Robbins & Kumar Basic Pathology (Robbins Pathology), p. 423–424 — LCH clinicopathologic entities
• Goldman-Cecil Medicine, International Edition — Posterior Pituitary and Diabetes Insipidus chapter, p. 2418–2423
• Goldman-Cecil Medicine — LCH and infiltrative disorders of the pituitary, p. 2423

Is it serious?

Is it curable?

What gives real hope for Raj specifically?

"Patients carrying sensitive mutations in BRAF or MAP2K1... show remarkable responses to inhibitors of RAF or MEK1."

What does "not fully curable" mean in some cases?

• Diabetes insipidus may be permanent even if LCH is brought under control. The pituitary damage sometimes does not reverse. But desmopressin manages it so effectively that most patients live completely normal lives with it — they just take a daily tablet or spray.
• A small number of patients (~10%) can develop a complication called neurodegeneration years later. Doctors watch for this with regular MRI follow-up.
• The risk of certain blood cancers (leukemia, lymphoma) is slightly higher in LCH patients over a lifetime — which is why long-term follow-up is important.

The bottom line for your family

MRI Brain Report — What It Shows (Raj, 25M, 30 April 2026)

What Was Found

• Multiple lytic (bone-destroying) lesions in the right frontal bone (front of skull) and right occipital bone (back of skull)
• These lesions are heterogeneously enhancing on contrast — meaning they light up with contrast dye, which indicates active, vascular disease (not old/healed lesions)
• The largest lesion measures 23.2 × 11.8 mm (~2.3 cm) in the right occipital bone — that is substantial
• The lesions are infiltrating into adjacent soft tissue — meaning LCH has broken through the bone and is spreading into the scalp/soft tissue layer on top

• These are scarring/healing changes from prior treatment (likely from his biopsy or curettage done ~1 year ago) — this is expected and not worrying

• Brain parenchyma (brain tissue itself) — normal
• Cerebellum, brainstem — normal
• Ventricles — normal
• Sella and parasellar areas — normal (this is the pituitary gland region)
• No restricted diffusion (rules out stroke/abscess)
• No blooming on GRE (rules out bleeding)

What This Means Clinically

One Important Nuance — The Pituitary

• Central DI in LCH is caused by infiltration of the pituitary stalk (the connector between hypothalamus and pituitary), not the pituitary gland body itself
• Pituitary stalk thickening or loss of the posterior pituitary bright spot on T1-weighted MRI is the classic LCH finding — but this requires dedicated pituitary protocol MRI (thin cuts through the sella), which this standard brain MRI may not have captured in detail
• His symptoms of polydipsia + polyuria + hypernatremia (Na 145.3) are still strongly suggestive of DI regardless

Bottom Line for the Family

1. This MRI confirms LCH relapse with active skull lesions — the disease is back and active in the bones of his skull
2. The forehead swelling is a direct LCH lesion breaking through bone into soft tissue
3. The brain tissue itself is not invaded — this is a relief
4. The MRI findings, combined with his blood results and symptoms, make a strong, complete case for LCH relapse — no ambiguity remains
5. This report needs to go to a haematologist/oncologist today or tomorrow — it is the final piece confirming the diagnosis, and systemic treatment (cladribine ± cytarabine, or BRAF-targeted therapy if BRAF V600E positive) needs to be started

Is It Dangerous? Can Raj Recover? How Long Is Treatment?

Is It Dangerous?

• Raj has multisystem LCH (skull bones + likely pituitary involvement) — this is a relapse, which occurs in 20–50% of LCH patients. Relapse is a known and expected part of this disease, not a sign that everything has gone wrong.
• The MRI shows no brain tissue invasion — this is very important. The lesions are in the bone and soft tissue of the skull, not inside the brain itself.
• His brain, cerebellum, and brainstem are completely normal on MRI.
• His liver, spleen, and bone marrow are not mentioned as affected — these are the "risk organs" that would make the disease more dangerous. Based on what we know, he may not have risk organ involvement, which puts him in a better category.

Can He Recover?

"Responses to a variety of second-line therapies have been documented... BRAF inhibitors produce remarkable and durable responses in patients with BRAF V600E mutations... cure is the goal of therapy."

How Long Will Treatment Last?

• First 2–4 weeks: Diagnosis confirmed, BRAF testing done, treatment started
• 3–6 months: If responding well, bone lesions shrink, symptoms improve significantly
• 6–12 months: Main treatment course completed
• After treatment: Regular follow-up scans every 3–6 months for 2–3 years
• Some patients need maintenance therapy for 1–2 years after the initial course

What About the Diabetes Insipidus?

The Most Important Message

Raj is 25 years old. He responded to treatment before. His disease is in bone — not in vital organs. He does not have brain invasion. He has modern targeted therapies available to him that did not exist 10 years ago. With the right treatment team, full functional recovery is realistic.

PET-CT (Jan 7, 2026) — What It Showed

Key Findings from the Report:

• Non-FDG avid lytic sclerotic lesions in right parietal bone, left frontal bone, and left iliac bone
• Mild diffuse FDG avidity in axial and appendicular skeleton — reported as "Reactive bone marrow"

"Non FDG avid lytic sclerotic skeletal lesions. No other evidence of metabolically active disease in present whole body scan." "Compared to previous PET-CT dated 28/01/2025, scan findings more or less consistent — suggestive of stable disease."

Correlation: January 2026 PET-CT vs. April 2026 MRI

The Critical Difference — Were They Different Lesions?

1. January 2026 — Residual / Treated Lesions (NOT active)

• The lesions seen on PET-CT in January 2026 (right parietal, left frontal, left iliac) were non-FDG avid — meaning they had no active metabolic activity. In LCH language, this means they were "healed" or "sclerotic" post-treatment lesions — essentially bone scars from previous LCH activity, not live disease.
• The report itself said "stable disease" — consistent with the prior scan from January 2025.
• Raj was still on cytarabine chemotherapy at the time of this scan — the treatment appeared to be working, as no metabolic activity was detected.

2. April 2026 MRI — NEW Active Lesions (RELAPSE)

• The MRI now shows enhancing lesions in right frontal and right occipital bones — sites not even mentioned in the January 2026 PET-CT
• These are in different locations from the January 2026 residual lesions (right parietal / left frontal)
• They are heterogeneously enhancing on contrast — the MRI contrast enhancement confirms active blood supply and active disease, which FDG-PET would also have shown as "hot" if done today
• The soft tissue scalp extension is completely new — not present in January

3. The Left Frontal "Post-procedural/Scarring Changes" on MRI

• The MRI mentions "post-procedural/scarring changes in left frontal and parietal regions" — these correspond exactly to the old, treated, non-FDG avid lesions seen on the January 2026 PET-CT
• This confirms those old lesions are healed/treated — the MRI is validating what the PET-CT showed in January

Timeline Reconstruction

What This Means Clinically

1. The January 2026 PET-CT was NOT falsely negative — it correctly showed that the existing lesions were treated and stable. However, LCH can emerge at new sites rapidly, especially after treatment ends. This is called reactivation at new sites, which is a recognized pattern in LCH.
2. The current relapse is at NEW bone locations (right frontal + right occipital) that were not diseased in January 2026 — this is a true new relapse, not a failure to detect old disease.
3. The PET-CT limitation noted — the report itself says: "Whole Body FDG PET/CT is not very sensitive for brain metastasis." This is relevant because early skull base and pituitary stalk LCH lesions may be missed on FDG-PET; contrast-enhanced MRI is more sensitive for skull/CNS LCH.
4. Good news from the PET-CT: As of January 2026, there was no involvement of liver, spleen, lungs, or bone marrow as active disease — this places Raj in the low-risk multisystem category, which has a very favorable prognosis (~99% survival).

Summary Answer to Your Question

Were the current active lesions different from the past lesions?

• Past lesions (Jan 2026): Right parietal + left frontal + left iliac — non-FDG avid, non-enhancing sclerotic scars — treated/healed disease
• Current lesions (Apr 2026): Right frontal + right occipital — heterogeneously enhancing, soft tissue extension — NEW active relapse at entirely new sites

Report: Apollo Hospitals, April 30, 2026 — Raj's Urine & Serum Biochemistry

The Numbers at a Glance

What This Report Means — Plain Language

1. Urine Osmolality of 65 mosmol/kg = DIAGNOSTIC of Diabetes Insipidus

• Normal kidneys, when the body is even slightly dehydrated or sodium is high, will concentrate urine to >800–1200 mosmol/kg — producing dark, concentrated urine
• Raj's serum sodium is 143 mmol/L — at the high end, meaning his body is slightly "dry" / concentrated
• Despite this, his kidneys are producing urine at only 65 mosmol/kg — almost as dilute as plain water (water = ~0 mosmol/kg)
• This is the textbook definition of Central Diabetes Insipidus: the brain (posterior pituitary/hypothalamus) is NOT releasing ADH (antidiuretic hormone), so the kidneys cannot concentrate urine no matter how much the body needs water conserved

2. Urine Sodium of 11 mmol/L — Confirms Massive Water Loss, NOT Salt Loss

• The lab's own interpretation says: Normal >20, Low <10, High >30
• Raj's value is 11 — borderline low
• This tells us: the kidneys are losing pure water, not sodium — characteristic of DI
• In contrast, if kidneys were damaged (nephrogenic DI), sodium would also be spilled
• This pattern (very low urine osmolality + preserved sodium handling) = Central DI from ADH deficiency

3. Why Is Urine Creatinine Also Low (14 mg/dL)?

• Normal urine creatinine is 25–400 mg/dL
• Raj's low value confirms his urine is massively dilute — high flow, low concentration
• This is not kidney damage; it's simply that huge volumes of dilute water are being poured out, diluting everything in the urine

How This Confirms Our Earlier Diagnosis

How DI Affects LCH Treatment & Healing

1. Dehydration impairs chemotherapy clearance — cytotoxic drugs (cladribine, cytarabine) depend on adequate kidney perfusion to be excreted safely. If Raj is chronically dehydrated from uncontrolled DI, drug toxicity risk increases.
2. Electrolyte instability — uncontrolled DI can cause dangerous sodium swings, which affect heart rhythm, brain function, and medication dosing.
3. Fatigue and weakness worsen — DI-related dehydration + hypogonadism (testosterone 126 ng/dL) compound each other in causing the severe weakness he's experiencing.
4. Pituitary DI in LCH is usually permanent — once ADH neurons are destroyed, they do not regenerate. But this does NOT mean untreatable. Desmopressin (DDAVP) fully replaces ADH and is a lifelong, safe, effective therapy.
5. Treating LCH (the root cause) prevents further pituitary damage — every day of active LCH lesions risks more hypothalamic destruction. Getting systemic therapy started urgently is critical to preventing worsening DI or loss of other pituitary hormones (growth hormone, cortisol, thyroid).

Questions to Ask the Endocrinologist Today

🔑 About Diabetes Insipidus

1. "Raj's urine osmolality is 65 mosmol/kg with serum sodium of 143. Can we start desmopressin (DDAVP) today? What dose and route do you recommend — intranasal or oral?"
2. "How do we adjust the DDAVP dose and monitor it safely at home? What urine output volume should we target?"
3. "What are the signs of over-treatment (water intoxication / low sodium) that we should watch for?"
4. "Should we measure serum sodium at home with a portable test, or come in weekly? How often should we check labs?"

🔑 About Full Pituitary Function Assessment

1. "The MRI shows LCH lesions near the skull. We need a dedicated pituitary MRI with thin cuts and contrast — can you order this or should the oncologist order it?"
2. "Can you check LH, FSH, early morning cortisol, ACTH, IGF-1, and prolactin today — to assess all pituitary axes?" (Raj's testosterone was already 126 ng/dL — severely low — but we need to know WHY: is LH/FSH also low?)
3. "Is there any cortisol deficiency (adrenal insufficiency)? This would be dangerous and needs immediate replacement."
4. "Does Raj need a water deprivation test or copeptin test to formally confirm central DI, or is his urine osmolality of 65 already sufficient for diagnosis?"

🔑 About Coordination with Oncology

1. "Raj has confirmed LCH relapse on the April 30 MRI. How urgently does systemic chemotherapy/targeted therapy need to start, and should desmopressin be started first or simultaneously?"
2. "If Raj is started on vemurafenib or cladribine, do any of those drugs affect pituitary function or interact with DDAVP?"
3. "Should we test for BRAF V600E mutation now, and does the endocrinologist want to be in the loop on targeted therapy decisions?"

🔑 About Testosterone / Hypogonadism

1. "Testosterone was 126 ng/dL — very low for a 25-year-old. Is this from pituitary damage (low LH/FSH) or primary testicular failure? Can we confirm with LH + FSH today?"
2. "When should testosterone replacement be started — before or after LCH treatment begins?"

Immediate Next Plan (Priority Order)

The Bottom Line for Your Family

Questions Raj Can Ask the Endocrinologist

About What Is Happening to His Body

1. "Doctor, can you explain in simple terms why I am urinating so much and always thirsty? Is it because my brain is not making a hormone?"
2. "Is this condition — the excessive urination — related to my LCH, or is it a separate problem?"
3. "My urine test shows osmolality of 65 — is that confirmed diabetes insipidus? What does that number mean for me?"
4. "Is there any damage to my pituitary gland? Can we check all the hormones my pituitary is supposed to make?"

About Starting Treatment Today

1. "Can I start the medicine for this today? I have been suffering with constant thirst and going to the toilet every hour — it is exhausting."
2. "Which form of desmopressin is better for me — the nasal spray, the tablet, or the melt-under-tongue tablet? Which is easiest to use daily?"
3. "How quickly will the medicine work? Will I feel better within a day or two?"
4. "What is the right dose for me, and how do I know if it is working? How much urine output per day is the target?"

About Safety and Monitoring

1. "What happens if I take too much of this medicine — is there a risk of my sodium dropping dangerously low? What symptoms should I watch out for?"
2. "How often do I need blood tests to check my sodium level once I start this medicine?"
3. "Can I drink water freely, or do I need to restrict how much I drink after starting desmopressin?"
4. "If I forget a dose one night, what should I do — take it the next morning or skip it?"

About His Hormones (Testosterone / Energy / Weakness)

1. "My testosterone came back very low at 126. Is that because my pituitary is not sending the signal to my testes? Can we check LH and FSH today?"
2. "Could low testosterone be the reason I feel so weak, have no appetite, and feel depressed? Can treating it help me feel stronger?"
3. "When can testosterone replacement start — before or after my cancer treatment begins?"

About Living with This Long-Term

1. "Will I need to take desmopressin for the rest of my life, or can it recover once LCH is treated?"
2. "I am only 25 years old. Will this condition affect my ability to work, exercise, travel, or live normally?"
3. "Will this affect my fertility or ability to have children in the future?"
4. "Are there any foods, drinks, or activities I need to avoid while on this medicine?"

About Coordination with Oncology

1. "My MRI from today shows active LCH lesions in my skull bones. How urgently do I need to see an oncologist? Can you refer me or speak to the cancer team directly?"
2. "Will the chemotherapy or targeted therapy for LCH affect my pituitary hormones further? Should I be getting hormone checks during that treatment?"
3. "Should I carry a medical alert card or letter saying I have Central Diabetes Insipidus — especially important if I ever need surgery or go to an emergency room?"

The Most Important Single Question

"Doctor, I have confirmed LCH relapse with active skull lesions on MRI today, and my urine osmolality is 65 — which means my pituitary is being damaged right now. Can we start desmopressin today AND refer me to oncology this week so the root cause is treated before more pituitary damage happens?"

A Tip for the Consultation

• How many times he urinates per day/night
• Roughly how many litres of water he drinks per day
• How long the excessive thirst/urination has been going on
• His current weakness, weight loss, and poor appetite

The Core Logic: Why the Doctor Said Avoid Watermelon

If Raj takes too much free water (from drinks OR water-rich foods), his kidneys will retain it, his sodium will DROP dangerously low — a condition called hyponatremia, which can cause confusion, seizures, or worse.

Fruit-by-Fruit Breakdown

Ice Apple (Nungu) — Can Raj Eat It?

Why Ice Apple Is Not Forbidden

• Its water content (~87%) is similar to papaya (~88%), which the doctor already approved
• It contains natural electrolytes — potassium and sodium — which actually help maintain Raj's electrolyte balance
• It is low in sugar (only ~10g carbs per serving) — not harmful for his borderline HbA1c
• It is cooling, easily digestible, and good for someone with poor appetite — Raj struggles to eat, so gentle foods like this help
• It has no diuretic effect of its own

Why Portion Size Matters

• Watermelon is avoided not just because of water content alone — it is because people eat large amounts of it (2–3 thick slices = nearly 500 mL of water)
• Ice apple pieces are naturally small and limited — 1–2 nungu pieces = roughly 50–80 mL of water equivalent — which is very manageable
• If Raj eats 4–5 pieces at once, it becomes similar to drinking a cup of water — that is when it becomes a concern

Practical Rules for Raj — Fruits & Water Management

✅ Safe to Eat (in normal portions)

• Papaya (as the doctor said)
• Ice apple / Nungu — 1 to 2 pieces at a time
• Banana — low water (~75%), good potassium, good calories for weak patients
• Mango — ~83% water, eat half a small mango at a time
• Guava — ~81% water, good Vitamin C, small portions fine
• Chikoo (Sapota) — good calories, low water

⚠️ Eat with Caution (small portions only)

• Ice apple — max 2 pieces at once
• Oranges / Mosambi — ~87% water, limit to 1 fruit
• Grapes — ~81% water, limit to a small handful

❌ Avoid or Strictly Limit

• Watermelon — ~96% water (as doctor said)
• Muskmelon / Kharbooja — ~90% water, similar risk to watermelon
• Cucumber as a large snack — ~96% water
• Coconut water / Nariyal pani — high free water, can disturb sodium balance quickly — ask the doctor specifically about this

The Most Important Rule of All

• Drink when genuinely thirsty — not out of habit or anxiety
• Do not force extra fluids thinking more water is healthier
• Count fruits with high water content as part of total fluid intake
• Monitor for symptoms of low sodium: headache, nausea, confusion, puffiness around the eyes in the morning — if any of these appear, check sodium immediately

Simple Summary for the Family

Ice apple (nungu) is safe for Raj — 1 to 2 pieces at a time. It is actually a good food for him because it is easy to eat, has natural electrolytes, and helps with his poor appetite. Just don't eat it in large quantities (4–5+ pieces at once), because the water load becomes too much — same reason watermelon is avoided. Papaya is excellent as the doctor recommended. When in doubt about any fruit or food, ask: "How much water am I drinking through this food?" — that is the real question with Central DI on desmopressin.

OSCE QUESTION — VASCULITIS

Clinical Scenario

MODEL ANSWER

(a) Diagnosis and Differentials (3 marks)

1. Polymyalgia Rheumatica (PMR) — closely associated with GCA; presents with shoulder/pelvic girdle stiffness in the same age group with elevated ESR. However, PMR alone does not cause jaw claudication or temporal artery changes.
2. Trigeminal neuralgia or tension headache — can cause unilateral head pain but lacks the systemic features, jaw claudication, and arterial changes seen here.

(b) Pathophysiology (4 marks)

1. Antigen trigger: An unknown antigen (possibly infectious or endogenous) activates dendritic cells in the adventitia of the vessel wall. These present antigen to CD4+ T-helper cells.
2. T-cell activation and granuloma formation: Activated Th1 and Th17 cells infiltrate the vessel wall — from adventitia inward through the media to the intima. Macrophages are recruited and fuse to form multinucleated giant cells, producing granulomas within the vessel media.
3. Cytokine cascade: Giant cells and macrophages secrete IL-1, IL-6, TNF-alpha, and metalloproteinases, causing smooth muscle cell destruction in the media, fragmentation of the internal elastic lamina, and vessel wall inflammation.
4. Intimal hyperplasia and luminal narrowing: In response to injury, the intima undergoes reactive hyperplasia, producing progressive luminal narrowing and ischaemia downstream. In the temporal artery this causes the pulselessness, tenderness, and headache. If the ophthalmic artery or posterior ciliary artery is involved, sudden irreversible blindness results.
5. Systemic inflammation: Elevated IL-6 drives the acute-phase response, explaining the markedly raised ESR, CRP, fatigue, and weight loss.

(c) Most Important Immediate Step (3 marks)

(d) Diagnostic Confirmation (2 marks)

• A segment of at least 1–2 cm of the temporal artery is excised (longer sample reduces false negatives from skip lesions).
• Histology shows: transmural granulomatous inflammation, multinucleated giant cells, fragmentation of the internal elastic lamina, and intimal hyperplasia.
• Sensitivity is ~85–90%; a negative biopsy does NOT exclude GCA if clinical suspicion is high ("skip lesions").

(e) Treatment Plan and Complication if Untreated (3 marks)

Quick Recall Summary